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Chemotherapy-induced senescence, an adaptive mechanism driving resistance and tumor heterogeneity
Open accessAbstract
Senescence is activated in response to chemotherapy to prevent the propagation of cancer cells. In transformed cells, recent studies have shown that this response is not always definitive and that persistent populations can use senescence as an adaptive pathway to restart proliferation and become more aggressive. Here we discuss the results showing that an incomplete and heterogeneous senescence response plays a key role in chemotherapy resistance. Surviving to successive chemotherapy regimens, chronically existing senescent cells can create a survival niche through paracrine cooperations with neighboring cells. This favors chemotherapy escape of premalignant clones but might also allow the survival of adjacent clones presenting a lower fitness. A better characterization of senescence heterogeneity in transformed cells is therefore necessary. This will help us to understand this incomplete response to therapy and how it could generate clones with increased tumor capacity leading to disease relapse.
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“Crucially to our findings, incomplete and heterogeneous senescence response of cancer cells contributes to chemotherapy resistance [53].”
From Identification of a novel gene signature predicting response to first-line chemotherapy in BRCA wild-type high-grade serous ovarian cancer patients (2022) · cites this paper as [53]
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Metadata
- Authors
- Guillon, J., Petit, C., Toutain, B., Guette, C., Lelièvre, E., & Coqueret, O.
- Affiliations
- Inserm (FR)
- Corresponding author
- Coqueret, Olivier
- Venue
- Cell Cycle
- Publisher
- Informa UK Limited
- Published
- 2019-08-09
- Volume
- 18
- Issue
- 19
- Pages
- 2385-2397
- ISSN
- 1538-4101 (ISSN-L)
- 1551-4005
- PMC
- PMC6738909
- OpenAlex
- W2966996218
- Cited by
- 102
- References
- 72
- Citations by year
- 2026: 9 · 2025: 18 · 2024: 20 · 2023: 24 · 2022: 11 · 2021: 13 · 2020: 6 · 2019: 1
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cell Cycle (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- Ligue Contre le Cancer (NA)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Telomeres, Telomerase, and Senescence
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Keywords
- chemotherapy-induced senescence, chemoresistance, tumor heterogeneity, senescence escape, paracrine signaling, recurrence, senescent cells, tumor cell proliferation
- MeSH terms
- Antineoplastic Agents, Clone Cells, Humans, Neoplasm Recurrence, Local, Neoplasms, Signal Transduction, Oncogene Proteins, Gene Expression Regulation, Neoplastic, Cellular Senescence, Apoptosis, Drug Resistance, Neoplasm, Tumor Suppressor Proteins, Cell Proliferation
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